Cellular and molecular mechanisms of Notch signal in pulmonary microvascular endothelial cells after acute lung injury

Abstract This study focused on the effect and mechanism of Notch signal on pulmonary microvascular endothelial cells (PMVECs) following acute lung injury. PMVECs were cultured in vitro and randomly divided into eight groups. Grouping was based on whether cells were co-cultured with T cells (splenic...

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Main Authors: Zheng Yang, Jilin Ma, Zhihui Li, Jie Wang, Zhanli Shi
Format: Article
Language:English
Published: Associação Brasileira de Divulgação Científica 2023-12-01
Series:Brazilian Journal of Medical and Biological Research
Subjects:
Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2023000100698&tlng=en
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author Zheng Yang
Jilin Ma
Zhihui Li
Jie Wang
Zhanli Shi
author_facet Zheng Yang
Jilin Ma
Zhihui Li
Jie Wang
Zhanli Shi
author_sort Zheng Yang
collection DOAJ
description Abstract This study focused on the effect and mechanism of Notch signal on pulmonary microvascular endothelial cells (PMVECs) following acute lung injury. PMVECs were cultured in vitro and randomly divided into eight groups. Grouping was based on whether cells were co-cultured with T cells (splenic CD4+T cells were isolated using MACS microbeads) and the level of Notch expression: Normal group and Normal+T cells group, Model group and Model+T cells group, Notch low-expression group and Notch low-expression+T cells group, and Notch overexpression group and Notch overexpression+T cells group. Except for the Normal group and Normal+T cells group, all other groups were treated with 500 μL lipopolysaccharide (1 μg/mL). The expression of VE-cadherin and Zo-1 protein in the Model group (with or without T cells) was lower than that in the normal group (with or without T cells), their expression in the Notch low-expression group (with or without T cells) was significantly increased, and their expression in the Notch overexpression group (with or without T cells) was significantly decreased. Compared with the normal+T cells group, the number of Treg cells in the Notch low-expression+T cells group decreased significantly (P<0.01). The number of Th17 cells in the Notch overexpression+T cells group was higher than that in the Model+T cells group (P<0.01), while the number of Treg cells decreased (P<0.01). Our results demonstrated that activated Notch signal can down-regulate the expression of the tight junction proteins VE-Cadherin and Zo-1 in PMVECs and affect Th17/Treg immune imbalance. Autophagy was discovered to be involved in this process.
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spelling doaj.art-9d4847c8d75b40568b7b5b247ead9b7d2023-12-26T08:30:35ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research1414-431X2023-12-015610.1590/1414-431x2023e12888Cellular and molecular mechanisms of Notch signal in pulmonary microvascular endothelial cells after acute lung injuryZheng Yanghttps://orcid.org/0000-0003-4940-9678Jilin Mahttps://orcid.org/0000-0001-9168-6068Zhihui Lihttps://orcid.org/0000-0001-9983-1610Jie Wanghttps://orcid.org/0009-0005-3909-4395Zhanli Shihttps://orcid.org/0000-0002-5824-3908Abstract This study focused on the effect and mechanism of Notch signal on pulmonary microvascular endothelial cells (PMVECs) following acute lung injury. PMVECs were cultured in vitro and randomly divided into eight groups. Grouping was based on whether cells were co-cultured with T cells (splenic CD4+T cells were isolated using MACS microbeads) and the level of Notch expression: Normal group and Normal+T cells group, Model group and Model+T cells group, Notch low-expression group and Notch low-expression+T cells group, and Notch overexpression group and Notch overexpression+T cells group. Except for the Normal group and Normal+T cells group, all other groups were treated with 500 μL lipopolysaccharide (1 μg/mL). The expression of VE-cadherin and Zo-1 protein in the Model group (with or without T cells) was lower than that in the normal group (with or without T cells), their expression in the Notch low-expression group (with or without T cells) was significantly increased, and their expression in the Notch overexpression group (with or without T cells) was significantly decreased. Compared with the normal+T cells group, the number of Treg cells in the Notch low-expression+T cells group decreased significantly (P<0.01). The number of Th17 cells in the Notch overexpression+T cells group was higher than that in the Model+T cells group (P<0.01), while the number of Treg cells decreased (P<0.01). Our results demonstrated that activated Notch signal can down-regulate the expression of the tight junction proteins VE-Cadherin and Zo-1 in PMVECs and affect Th17/Treg immune imbalance. Autophagy was discovered to be involved in this process.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2023000100698&tlng=enAcute lung injury (ALI)NotchInflammatory responseTh17TregAutophagosome
spellingShingle Zheng Yang
Jilin Ma
Zhihui Li
Jie Wang
Zhanli Shi
Cellular and molecular mechanisms of Notch signal in pulmonary microvascular endothelial cells after acute lung injury
Brazilian Journal of Medical and Biological Research
Acute lung injury (ALI)
Notch
Inflammatory response
Th17
Treg
Autophagosome
title Cellular and molecular mechanisms of Notch signal in pulmonary microvascular endothelial cells after acute lung injury
title_full Cellular and molecular mechanisms of Notch signal in pulmonary microvascular endothelial cells after acute lung injury
title_fullStr Cellular and molecular mechanisms of Notch signal in pulmonary microvascular endothelial cells after acute lung injury
title_full_unstemmed Cellular and molecular mechanisms of Notch signal in pulmonary microvascular endothelial cells after acute lung injury
title_short Cellular and molecular mechanisms of Notch signal in pulmonary microvascular endothelial cells after acute lung injury
title_sort cellular and molecular mechanisms of notch signal in pulmonary microvascular endothelial cells after acute lung injury
topic Acute lung injury (ALI)
Notch
Inflammatory response
Th17
Treg
Autophagosome
url http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2023000100698&tlng=en
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AT zhihuili cellularandmolecularmechanismsofnotchsignalinpulmonarymicrovascularendothelialcellsafteracutelunginjury
AT jiewang cellularandmolecularmechanismsofnotchsignalinpulmonarymicrovascularendothelialcellsafteracutelunginjury
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